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La liberación de 5-HT en el núcleo accumbens rescata los déficits sociales en el modelo de autismo de ratón

Jessica J Walsh¹, Daniel J Christoffel¹, Boris D Heifets²

¹Nancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford, CA, USA.

|August 10, 2018

Resumen

Alterar la liberación de serotonina de células cerebrales específicas en ratones tiene un impacto bidireccional en el comportamiento social. Este hallazgo ofrece nuevos objetivos terapéuticos para el trastorno del espectro autista

Área de la Ciencia:

La neurociencia
La genética
Ciencias del comportamiento

Sus antecedentes:

El trastorno del espectro autista (TEA) se caracteriza por déficits en la interacción social.
Los mecanismos neuronales subyacentes de la sociabilidad siguen siendo en gran medida desconocidos, lo que dificulta el desarrollo de una terapia efectiva.

Objetivo del estudio:

Investigar el papel de la señalización de la serotonina (5-HT) en el núcleo accumbens en la modulación del comportamiento social.
Explorar el impacto de las alteraciones genéticas asociadas con el TEA en las vías 5-HT y la sociabilidad.

Principales métodos:

Utilizó un modelo de ratón con una deleción en la región sinténica del cromosoma 16p11.2, una causa genética de TEA.
Empleó optogenética para modular la actividad de las neuronas dorsal de 5-HT.
Evaluó el comportamiento social y midió la actividad neuronal 5-HT.

Principales resultados:

La deleción genética en las neuronas 5-HT alteró el comportamiento social y redujo la actividad neuronal.
La activación optogenética de las neuronas dorsal rafe 5-HT rescató estos déficits sociales.
El efecto de rescate fue dependiente e imitado por la activación del receptor 5-HT1b en el núcleo accumbens.

Conclusiones:

La liberación de serotonina de las neuronas dorsal raphe que actúan en el núcleo accumbens juega un papel crítico en la regulación del comportamiento social.
Dirigirse a esta vía 5-HT en el núcleo accumbens puede ofrecer una nueva estrategia terapéutica para los déficits sociales en ASD.

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